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CGS21680 significantly upregulates CD39 and CD73 expression. CGS21680 accelerates the adenosine triphosphate (ATP) hydrolysis and adenosine generation[1]. CGS21680 (10 nM) alone shows only small survival activity, but the activity is significantly enhanced by the addition of a phosphodiesterase inhibitor, IBMX. The survival activity of CGS21680 on cultured motoneurons is exerted by mixed effects of the adenylate cyclase-cAMP-PKA pathway and the transactivation of neurotrophin receptors[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.


CGS21680 (1 mg/kg/i.p.) intervention promotes the development of EAN. CGS21680 exacerbates experimental autoimmune neuritis in Lewis rats induced with bovine peripheral myelin. The exacerbation is accompanied with reduced CD4+ Foxp3+ T cells, increased CD4+ CXCR5+ T cells, B cells, dendritic cells and antigen-specific autoantibodies, which is possibly due to the inhibition of IL-2 induced by CGS21680[2]. CGS21680 (0.1 mg/kg, i.p.) transiently increases heart frequency but does not modify blood pressure of rat, and does not modify either heart frequency or blood pressure at 0.01 mg/kg. Following transient MCAo, CGS21680 at both doses protects from neurological deficit from the first day up to 7 days thereafter. At this time, it has reduced microgliosis, astrogliosis and improved myelin organization in the striatum and cytoarchitecture of the ischemic cortex and striatum. Two days after transient MCAo, CGS21680 has reduced the number of infiltrated granulocytes into the ischemic tissue[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.


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Please store the product under the recommended conditions in the Certificate of Analysis.


10×106 MNCs from each group are re-suspended in 2 mL RPMI 1640. Cell suspensions are added with carboxy-fluorescein diacetate, succinimidyl ester (CFSE, final concentration 2.5 μM) and thoroughly mixed. After incubation in the dark for 15 min at 37°C, the staining process is quenched by adding 10 mL ice-cold complete RPMI 1640 (containing 10% FBS) and incubated on ice for 5 min. Then cells are washed twice with RPMI 1640. Cell pellets are re-suspended in complete RPMI 1640 (containing 10% FBS). The stained MNCs (1×106 cells/mL, 1 mL/well) are cultured in triplicates in 24-well culture plates in the dark at 37°C. Each well is supplied with 50 μL of Concanavalin A (ConA, final concentration 5 μg/mL) or 50 μL of P0 peptide (final concentration 10 μg/mL). 72 h later, cells are collected and stained with PE-labeled anti-rat CD4 antibody for 30 min at 4°C. Finally, cells are analyzed with a flow cytometer.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.


Female Lewis rats aged 6-8 weeks (body weight, 140-160 g) are housed under specific pathogen-free conditions in the local animal facility with free access to water and food. Administration of CGS21680 (at a dose of 1 mg/kg in PBS) starts on day 5 p.i. Rats in experimental group are injected with CGS21680 intraperitoneally (i.p.) every two days until the end of the experiments. Rats in control group are given equal volume of PBS in the same way. The doses (1 mg/kg/i.p.) and the treatment regimen (every two days, start on day 5 p.i.) are determined.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.


Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2


Keywords:

CGS 21680CGS21680CGS-21680Adenosine ReceptorP1 receptorInhibitorinhibitorinhibit


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